MEDICINE BLENDED ASSIGNMENT

    


MEDICINE BLENDED ASSIGNMENT (MAY 2021)

 01/06/2021

I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and comes up with a treatment plan.

This is the link of the questions asked regarding the cases:

 http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are my answers to the Medicine Assignment based on my comprehension of the cases.                        

                             ##1st CASE :

                           "NEUROLOGY "

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

1Q) WHAT IS MYELOPATHY HAND?

A)There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 

2Q)WHAT IS FINGER ESCAPE?

A)Finger escape:

   Also called as "Wartenberg's sign" is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".

3Q)WHAT IS HOFFMAN'S REFLEX?

A)Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free, way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.

                          ##2nd CASE :

                  "GASTROENTEROLOGY"

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

               

1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

A) Evolution of symptomatology :

H5 years back-1st episode of pain abdomen and vomitings 

Stopped taking alcohol for 3 years.

1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 

20 days back increased consumption of toddy intake

Since 1 week pain abdomen and vomiting

Since 4 days fever constipation and burning micturition

Anatomical localisation: Pancreas and left lung

As per above interpretations,

-Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

2Q) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

A) * Non pharmacological interventions : drains ( malecot & icd )

* Even i as a treating physician will follow the same approach

                          ##3rd CASE :

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

QUESTIONS :

1Q) What is the most probable diagnosis in this patient?

*Differential Diagnosis:

Ruptured Liver Abscess.

Organized collection secondary to Hollow viscous Perforation.

Organized Intraperitoneal Hematoma.

Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.

Grade 3 RPD of right Kidney

-The most probably diagnosis is that,there is abdominal hemorrhage. This can be the reason for abdominal distention, and that the blood which is aspirated. 

2Q) What was the cause of her death?

A)After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding),post surgical infection, or damage to internal organs. 

3Q) Does her NSAID abuse have something to do with her condition? How? 

A)NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. 

   Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.

                          ##4th CASE :

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

QUESTIONS :

1Q) Cause of liver abcess in this patient ?

A) Here ; the cause of liver abcess is :

* Amoebic liver abcess (ALA ) seen commonly in the tropics and is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.


•It has been argued that risk factors like socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.

• However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.

So thus, the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/

2Q) How do you approach this patient ?

A)  The patient is well managed by treating team ; and even I will follow the same approach.

3Q) Why do we treat here ; both amoebic and pyogenic liver abscess? 

A)  Considering the following factors:

    1) Age and gender of patient: 21 years (young) and male.

   2) Single abcess.

   3) Right lobe involvement.

•The abcess is most likely AMOEBIC LIVER ABSCESS … 

•But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and not recommended.

• And also by considering the risk factors associated with aspiration for pus culture:

1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.

2) Sometimes ; it has thin thinwall which may rupture if u aspirate.

3) Sometimes ; it is unliquefied.

•So by above mentioned factors how can u confirm whether it is pyogenic/ amoebic ?Thus we treat them both empirically in clinical practice.

https://academic.oup.com/bmb/article/132/1/45/5677141

4Q) Is there a way to confirm the definitive diagnosis in this patient?

A) Yes in a high resources, cause of liver abscess is usually determined using multiple diagnostic strategies such as,

•including blood cultures 

•entamoeba serology

• liver abscess aspirate for culture and molecular and antigen testing.

https://academic.oup.com/bmb/article/132/1/45/5677141

                        ##5th CASE :

                       "CARDIOLOGY"

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

QUESTIONS:

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans: *the anatomical localisation dor problem is BLOOD VESSELS;

* ETIOLOGY for patient problem;

    •The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.

•The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans: PHARMACOLOGICAL INTERVENTIONS;

1. TAB. Dytor ;

Mechanism: Through its action in antagonizing the effect of aldosterone. Spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

2. TAB. Acitrom ;

Mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting.

3. TAB. Cardivas ;

Mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.

4. INJ. HAI S/C ;

MECHANISM:Regulates glucose metabolism

•Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue.

5.TAB. Digoxin ;

Mechanism:Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:

   •Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,

  •An enzyme that controls the movement of ions into the heart.

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

3Q) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

Ans: Cardiorenal syndrome type 4 is seen in this patient.

4Q) What are the risk factors for atherosclerosis in this patient?

Ans: Effect of hypertention ,

   They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.

5Q) Why was the patient asked to get those APTT, INR tests for review?

Ans: APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

  •Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.

                        ##6th CASE:

                     "NEPHROLOGY"

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

QUESTIONS ;

1Q). What could be the reason for his SOB ?
ANS: Reason for his sob can be POST TURP SYNDROME: it occurs because of irrigation of absorption of large volumes of irrigation fluid during turp which can cause HYPONATREMIA,CARDIORESPIRATORY depression.

2Q) Why does he have intermittent episodes of  drowsiness ?
ANS: The hyponatremia which occurs as a part of post turp syndrome :low levels of sodium in the body can cause lethargy,fatigue and sleep. that cause drowsiness.

3Q). Why did he complaint of fleshy mass like passage in his urine?
ANS: Passing of fleshy like mass which is foamy can be because of infection where pus cells are more. like in the case of urinary tract infections.

4Q). What are the complications of TURP that he may have had?
ANS: complications of turp can be bladder injury,bleeding,hematuria,dysuria,infection. in this patient it can be infection as pus cells are seen

                         ##7th CASE :

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

QUESTIONS;

1Q)Why is the child excessively hyperactive without much of social etiquettes ?

A)Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention,expulsive activity and impulsivity, which are otherwise not appropriate for a person's age.

•For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).

2Q) Why doesn't the child have the excessive urge of urination at night time ?

A)Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition, like;

1. Psychosomatic disorder

2. Undiagnosed anxiety disorder 

3Q) How would you want to manage the patient to relieve him of his symptoms?

A)Bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.

•If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions thoseoccurring in the wall of the bladder

To treat attention deficit hyperactivity disorder:

•For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents.  Schools can be part of the treatment as well. 

•Methylphenidate: A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.

•Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.

                        ##8th CASE :

                 "GASTROENTEROLOGY"

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

QUESTIONS:

1Q)What is cause of patient's dyspnea?

A)The cause of dyspnea might be "PLEURAL EFFUSION."

2Q)Name possible reasons why patient developed hyperglycemia?

A)This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress

• The result of decreased synthesis and release of insulin is secondary to the damage of pancreatic β-cells .

•Elevated levels of catecholamines and cortisol.

3Q)What is reason for elevated LFT's? Is there any specific marker for alcoholic fatty liver disease?

A)LFT are increased due to hepatocyte injury,that is

•When the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher range of ALT can be a sign of liver damage.

•Elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.

The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to;

 (i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics.

 (ii) mitochondrial damage leading to increased release of mAST in serum.

4Q) What is line of treatment in this patient?

A) Plan of action and Treatment:

  *INVESTIGATIONS :

~ 24 hour urinary protein 

~ Fasting and Post prandial Blood glucose 

~ HbA1c 

~ USG guided pleural tapping 

  *TREATMENT :

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly.

                          ##9th CASE :

                          "NEUROLOGY"

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

QUESTIONS :

1Q).Does the patient's history of road traffic accident have any role in his present condition?

A)  NO

2Q) What are the signs of CVA?

A)   Signs of CVA can be:

       •Sudden numbness or weakness in arm or leg.                    especially one side of body
  • Sudden onset of dizziness , difficulty in walking
  • Sudden confusion ,trouble speaking or understanding speech
  • Sudden  headache with no known cause

3Q) What is drug rationale in the CVA?

 A)  Combination of thrombolytic  and neuroprotective therapy is given.


4Q) Does alcohol has any role in his attack?

 A)As the patient is a chronic alcoholic, it is possible that alcohol might have not played role in his attack  


5Q) Does hid lipid profile has any role in his attack?

A) Definitely ,high TGA And high cholesterol are risk factors for stroke 

                           ##10th CASE :

                         "CARDIOLOGY"

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1

QUESTIONS :

1Q)What can be the cause for her condition?     
   
   A)  THROMBOSIS AND INFARCTION

2Q) What are the reasons for cortical vein thrombosis
A)  1.BETA THALASSEMIA
        2.HEMOLYTIC ANEMIA
        3.HEAD TRAUMA
        4.IRON DEFICIENCY
        5.CANCER
        6.INTRACRANIAL HYPOTENSION    
   
3Q)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why? 
                          
 A)  The postictal state is the altered state of consciousness after an epileptic seizure. It usually lasts between 5 and 30 minutes, but sometimes longer in the case of larger or more severe seizures, and is characterised by drowsiness, confusion, nausea, hypertension, headache or migraine, and other disorienting symptoms.

4Q)What drug was used in suspicion of cortical venous sinus thrombosis?

A)   Anticoagulants.

                       ##11th CASE :

                       "CARDIOLOGY"

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.

QUESTIONS:


1Q).Why haven't we done pericardiocenetis in this patient?   

   A) As the condition is resolving, there is not need for pericardiocentesis
             
2Q) What are the risk factors for the developmemt of the heart failure in the patient?
    A)    •hypertension
             •CAD
             •DM
             •MEDICATIONS

3Q)What could be tha cause of hypotension in this patient?

  A) The venous return is low in this patient , there by cardiac output is also decreased due to which hypotension is observed in this patient.

                           ##12th CASE:

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html

QUESTIONS :

 1Q).What are the possible causes for heart failure in this patient?

Answer:
  • Diabetes mellitusDiabetic patients have an increased risk of developing heart failure because of the abnormal cardiac handling of glucose and free fatty acids (FFAs), and because of the effect of the metabolic derangements of diabetes on the cardiovascular system
  • Hyper tensionHigh blood pressure forces your heart to work harder to pump blood to the rest of your body. This causes part of your heart (left ventricle) to thicken. A thickened left ventricle increases your risk of heart attackheart failure and sudden cardiac death. Heart failure.
  • CKD stage 4: Damaged kidneys may release too much of an enzyme called renin, which helps to control blood pressure. This increases your risk for heart attack, congestive heart failure and stroke. 
  • Chronic alcoholicLong-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can't pump blood efficiently, the lack of blood flow disrupts all your body's major functions. This can lead to heart failure and other life-threatening health problems
  • Atrial fibrillationBy not getting enough oxygen to the body, afib can lead to heart and valve diseases, sleep apnea, and chronic fatigue. In addition, atrial fibrillation can lead to two potentially life-threatening conditions, congestive heart failure and stroke
  • COVID-19
2Q)What is the reason for anemia in this case?
Answer:
  • Red blood cells are made by the bone marrow. To get the marrow to make red blood cells, the kidneys make a hormone called erythropoietin, or EPO. When the kidneys are damaged, they may not make enough EPO. Without enough EPO, the bone marrow does not make enough red blood cells, and you have anemia.
  • Red blood cells are constantly turned over by the body, so too much red blood cell destruction can also lead to anemia. While alcohol and anemia are generally not thought to be related, drinking too much alcohol can lead to anemia.
  • Diabetes is the single most common cause of end-stage renal disease (1) and therefore the most common cause of renal anemia. In addition, anemia may be more common in diabetes (2) and develop earlier than in patients with renal impairment from other causes.
3Q).What is the reason for blebs and non healing ulcer in the legs of this patient?

Answer:
  •Leg ulcers are debilitating and greatly       reduce  patients' quality of life. The common causes are venous disease, arterial disease, and neuropathy. Less common causes are metabolic disorders, hematological disorders, and infective diseases.
  • Uncontrolled diabetes mellitus(Diabetic neuropathy)- Circulation of blood at the wound site is critical for wound healing. As a result of narrowed blood vessels, diabetic wound healing is impaired because less oxygen can reach the wound and the tissues do not heal as quickly.
  • Kidney failure
  • Pressure due to any shoes, etc.
  • Trauma
  • Hypertension
4Q). What sequence of stages of diabetes has been noted in this patient?

Answer:
According to case details he had crossed all stages of diabetes.

stage 1: defined as DCBD insulin resistance;
 stage 2: defined as DCBD prediabetes;
 stage 3: defined as DCBD type 2 diabetes;
 stage 4: defined as DCBD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events.

                                ##13th CASE:
                          "PULMONOLOGY"

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

QUESTIONS :

1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

ANS:  a) The evolution of symptomatology in the patient:

        > It begins with shortness of breath more commonly at work rather than at rest. Even the slight amount of pressure/work causes exertion resulting in shortness of breath.

       > Gradually, SOB is observed even at resting condition where it is progressed along with pedal edema.

       > Bronchiectasis (cough produced with mucus) is observed.

       > Then raise in blood pressure/hypertension in the lung arteries is seen.

       > Later, the right heart muscle weakens leading to the failure of heart on the right side.

b ) The anatomical localization for the problem is the lung (respiratory system) which later progresses towards the heart.

c ) The primary etiology of patient’s could be because of her occupation where she worked in the paddy fields. Working around the dust arousing from the fields may have caused COPD in the patient.

2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANS:   a ) Pharmacological interventions:

Inj AUGUMENTIN 1.2gm IV BO: It is used for treating short term bacterial infection in the case of acute exacerbation of COPD. It contains 2 different medicines that work together to kill the bacteria that cause infections. Amoxycillin works by stopping the growth of bacteria. Clavulanic acid is a beta-lactamase inhibitor that reduces resistance and enhances the activity of amoxicillin against the bacteria.  

> TAB. AZITHROMYCIN 500mg OD: Azithromycin kills certain bacteria and reduces inflammation in the lungs, which may help in reducing the number of lung attacks the patient has. It helps in reducing chest symptoms such as coughing, sputum (phlegm) and breathlessness.

Inj LASIX IV BO: Lasix (furosemide) is an anthranilic acid derivative that is used s strong diuretic to treat excessive fluid accumulation (edema). It is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes metabolic alkalosis

TAB PANTOP 40mg PO OD: Used for heatburn and chest pain.

Inj HYDROCORTISONE 100mg IV: Hydrocortisone is a corticosteroid. It is administered to reduce inflammation. This drug suppresses eosinophils present in the airway which are responsible for inflammation.

TAB PULMOCLEAR 100mg PO OD: It is a combnation of 2 medicines that helps the airways in the lungs stay open. It works by relxaing the muscles of these airways. This makes it easier for the air to get in and out. It also helps in loosening the thick mucus making easier to cough it out. It will relieve symptoms such as tightening of chest, wheezing, coughing and SOB.

Inj THIAMINE 1 amp in 100ml of NS: It is effective for treatment of congestive heart diseases and also for the increase in VO2 levels.

 

b ) Non pharmacological interventions:

HEAD END ELEVATION: It is a commonly used therapeutic intervention in mechanically ventilated patients associated with a reduction in the incidence of ventilator associated pneumonia. It improves oxygenation and hemodynamic performance.

O2 INHALATION: To maintain the spO2 above 92%

INTERMTTENT BiPAP: Bilevel Positive Airway Pressure ventilation is a noninvasive technique used to provide ventilator support to a spontaneously, but insufficiently, breathing patient using a facemask or nasalmask. With this mode of ventilation, BiPAP cycles between two levels of continuous positive airway pressure. This mode of ventilation has resulted in shorter duration of ventilation, less need of sedation and fewer complications. It is useful for the patients with COPD.

CHEST PHYSIOTHERAPY: The Airway Clearance Technique assists in sputum clearance in an attempt to reduce symptoms  and paroxysmal coughing, slow the decline in lung function, reduce exacerbation frequency and hasten the recovery from exacerbation.

3Q) What could be the causes for her current acute exacerbation?
ANS:  Recently, her HRTC showed signs of bronchiectasis. [A condition where bronchial tubes of lungs are permanently damaged, widened and thickened. These damaged air passages allow bacteria and mucus to build up and pool in the lungs blocking the airways] This could be a trigger factor for the current acute exacerbation.


4Q). Could the ATT have affected her symptoms? If so how?
ANS:  Yes. Empirical ATT resulted in generalized weakness. A week after ATT, pedal edema and facial puffiness is seen. Some cases of COPD maybe preventable by controlling the TB epidemic, early TB diagnosis and prompt initiation of appropriate anti-TB treatment. Follow-up care and early intervention for COPD maybe necessary for treated TB patients.

5Q).What could be the causes for her electrolyte imbalance?
ANS: Patients with COPD are susceptible mainly to hyponatremia (low levels of sodium ions). Chronic hypoxia and hypercapnia secondary to the underlying pulmonary illness, heart failure, use of bronchodilators or steroids, malnutrition during acute exacerbation are common contributing factors for electrolyte imbalance. Activation of Renin-angiotensin-aldosterone system and inappropriately elevated plasma arginine vasopressin in COPD may also cause electrolyte imbalance.  

                          ##14th CASE

                          "NEUROLOGY"

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

QUESTIONS:

1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS: a ) Evolution of symptomatology:

Ø 2-3 episodes of seizures, apparently with a gap of 8 months in between.

Ø Alcohol withdrawal symptoms associated with restlessness, sweating and tremors are observed

Ø Sudden onset of talking and laughing to himself was seen.

Ø Disability in lifting himself off the bed move around is seen.

Ø Later, short-term memory loss associated with not being able to recognize family members from time to time was observed.

    b ) Anatomical localization include the lower parts of the brain called thalamus and hypothalamus in Wernicke’s encephalopathy.

   c ) Primary etiology of the patient’s problem is thiamine deficiency due to excessive alcohol consumption. 

2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANSPharmacological interventions:

Ø IVF NS and RL: Intravenous normal saline is administered as a source for hydration as well as electrolyte balance whereas ringer’s lactate is used to treat dehydration.

Ø Inj THIAMINE 1amp: Thiamine injection is administered as there is a deficiency of thiamine in alcohol addicts.

Ø Inj LORAZEPAM: It is administered in this case to treat seizures of the patient. It binds to a type of GABA receptor and activates it in a similar way to GABA which leads to the inhibition of uncontrolled firing of neurons that causes seizures.

Ø TAB PREGAALIN 75mg/PO/BD: It is an antiepileptic drug. It is also used to treat neuropathic pain. It binds to alpha2-delta subunits and reduces the synaptic release of several neurotransmitters thus preventing the seizure.

Ø LACTULOSE 30ml/PO/BD: It is used in preventing and treating portal-systemic encephalopathy. Its chief mechanism of action is by decreasing the production and absorption of ammonia. It may also be helped in the improvement of mental status.

Ø Inj 2 AMPOULE KCl in 10NS: It is used in the treatment of hypokalemia, prophylaxis for hypokalemia, IV intermittent fusions.

Non pharmacological interventions:

Ø GRBS: General Random Blood Sugar test for detecting blood glucose levels.   


3Q) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

ANS:  Multiple alcohol withdrawals gradually leads to permanent alterations in GABA receptors which causes neurological damage. This is the reason why neurological symptoms appear later than earlier.

4Q) What is the reason for giving thiamine in this patient?
ANS:  Alcohol consumption leads to thiamine deficiency. This is due to poor nutrition causing decrease in essential vitamins. And also alcohol causes inflammation in stomach lining causing reduction in absorption of vitamins.   

5Q) What is the probable reason for kidney injury in this patient? 
ANS: Binge drinking alcohol causes high rise of alcohol content in blood causing kidneys to lose their function termed as acute kidney injury. Chronic alcohol abuse results in damage of kidney function leading to the leakage of proteins into the urine, commonly called as Albuminuria which is an early sign of kidney disease.

6Q). What is the probable cause for the normocytic anemia?
ANS: Heavy alcohol consumption cause generalized suppression of blood cell production and production of structurally abnormal blood cell precursors that cannot fully mature into functional cells. Defective RBCs are destroyed prematurely causing low number production of them resulting in normocytic anemia.


7Q) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
ANS: Chronic alcoholism can cause nutritional deficiencies and alcohol toxicity. These can inturn cause poor wound healing and problems with nerves (neuropathy). When sensory nerves in foot stop working, the foot can get injured and this leads to foot ulcers.

                        ##15th CASE

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

QUESTIONS :

1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS: a )  Evolution of symptomatology:

Ø Development of bilateral pedal edema with a gradual progression present in both sitting and standing positions.

Ø Sudden onset of palpitations, more during the night, are seen after 8 months of development of bilateral pedal edema.

Ø Aggravation of palpitations occurred during weight lifting and continuous speaking along with dyspnoea.

Ø Radiating pain from chest in the upper limb is observed along with chest heaviness

b ) Anatomical localization for the patient’s problem of Cervical spondylosis include  intervertebral discs present between cervical vertebrae. And that of recurrent hypokalemic paralysis include muscles of arms and legs.

c ) Dehydrated disks due to aging, generally by the age of 40, causes drying out and shrinking of spinal disks which allows more bone-on-bone contact between the vertebrae resulting in cervical osteoarthritis (spondylosis). As the patient’s age is 45, aging can be considered as the primary etiology.

2Q) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANS:The patient complained of sudden onset of aggravating palpitations. She was relieved on using medication. Diuretics (water pills) are administered for irregular heartbeat. Use of diuretics cause loss of water along with sodium and potassium ions resulting in hypokalemia.
Important risk factors for her hypokalemia include medications like diuretics which are being administered for palpitations.
3Q) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS: ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression in more severe hypokalemia. 
   Associated symptoms included in severe hypokalemia can result in arrhythmias and ventricular tachycardia.
                            
                           ##16th CASE :

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

QUESTIONS :


1Q). Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANSYes, there is a relation between occurrence of seizure and brain stroke. The mechanism involved is as follows: A stroke causes the brain to become injured. The injury to brain results in the formation of scar tissue which affects the electrical activity in brain. Disrupting the electrical activity can cause the occurrence of a seizure.


2Q). In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

ANSIn the recent episode, the seizure was tonic-clonic which is a grand mal seizure. Grand mal seizure causes a loss of consciousness and violet muscle contractions. It is caused by abnormal electrical activity throughout the brain. Previous episodes of seizures did not show tonic-clonic movements.

                               ##17th CASE

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
 
QUESTIONS :


1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

ANS: a ) Evolution of symptomatology:

The beginning symptom was giddiness which briefly subsided after rest.

Giddiness was associated with vomiting on the  same day

After being asymptomatic for 3 days,  sudden onset of giddiness appeared again which was progressive in severity while walking.

Bilateral hearing loss, aural fullness and presence of tinnitus were seen.

Association of 2-3 episodes of vomiting per day which were non projectile, non bilious containing food particles was observed.

H/o postural instability (unable to walk without support), tendency to fall while walking and swaying is present.

b ) Damage to unilateral cerebellar hemisphere causes ipsilateral cerebellar ataxia.

            c ) primary etiology of the patient’s problem is due to excessive consumption of alcohol.


2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS:  Pharmacological interventions:

TAB VERTIN 8mg PO TID: It is used to treat hearing loss as bilateral hearing loss is seen in the patient. It is a betahistin which improves the microcirculation of the inner ear. It works as antagonist of H3 receptors against which it has a strong effect.

Inj ZOFER 4mg IV/TID: It is used to prevent and manage nausea and vomiting.

TAB ATORVOSTATIN 40mg PO/HS & TAB ECOSPRIN 5mg: Both of these drugs are administered to prevent heart attacks and heart strokes as the patient past history shows denovo hypertension.

TAB MVT & THIAMINE 1amp in 100ml NSPO/BD:   Multivitamins and thiamine are administered as a source for essential vitamins as the patient is alcoholic.

*Non pharmacological interventions:

BP MONITORING: Since the patient is hypertensive, BP is monitored frequently.


3Q) Did the patients history of denovo HTN contribute to his current condition?
ANS: Yes, patient’s history of denovo HTN contributes to his current condition of CVA. The extra strain that high BP puts on the blood vessels may cause a weakened blood vessel to burst inside the brain, causing bleeding on and into surrounding tissues. This is called a hemorrhagic stroke and this is a type of cerebrovascular accident.

4Q) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
ANS: Patient’s alcoholism causes hemorrhagic stroke. That is because liver damage due to too much alcohol can stop liver from making substances which are responsible for blood clot. This causes the risk of having a stroke caused by bleeding in the brain which is called as hemorrhagic stroke
                            ##18th CASE

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

QUESTIONS :

1Q) What could have been the reason for this patient to develop ataxia in the past 1 year?
ANS The reason for ataxia in the patient maybe due to head trauma, where he reportedly mentioned about several falls on head which were left unattended. It could also be due to the alcohol intoxication as the patient is an addict since 3 years.

2Q) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANS Binge drinking alcohol causes low affinity of hemoglobin binding to oxygen leading to low levels of oxygen saturation. Deprived oxygen to the brain can cause Intracranial hemorrhage (ICH). As the patient was binge drinking alcohol 3hrs prior to the drowsiness, this could have been the reason for his IC bleed.
     Yes ,chronic alcoholism contributes to bleeding diathesis associated with impaired platelet function together with reduced platelet count.

                           ##19th CASE
    "INFECTIOUS DISEASE AND HEPATOLOGY"

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

QUESTIONS :


1Q). Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?What could be the cause in this patient ?
 ANS: yes, it could be due to intake of contaminated toddy.

2Q). What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
ANS:  According to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is for causation of  both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver which damages it in many different ways.

3Q). Is liver abscess more common in right lobe ?
ANS: yes right lobe is involved due to its more blood supply , As increase in blood supply increase intransportation of inflammaotory substances which increase in inflammation and formation of abscess.


4Q).What are the indications for ultrasound guided aspiration of liver abscess ?
ANS: Indications for USG guided aspiration of liver abscess
- amoebic liver abscess 
-Large abscess more than 6cms
- Left lobe abscess
-Caudate lobe abscess
-. Abscess which is not responding to drugs
-seronegative abscess

                             ##20th CASE :
                   " INFECTIOUS DISEASE"
(MUCORMYCOSIS,OPHTHALMOLOGY,OTORHINOLARYNGOLOGY)

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

QUESTIONS :

1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS: a ) Evolution of symptomatology:

• Hypertension since 3yrs.

• Fever associated with chills and rigors.

• Generalized weakness, facial puffiness and preorbital edema along with drowsiness.

•  Weakness of upper and lowerlimbs

• Diagnosis of Diabetic ketoacidosis.

               b ) Anatomical localization include nasal or palatine findings of mucormycosis including grey or reddish mucosa which will progress to black areas of eschar as necross ensues. Eschar maybe seen in nasal septum, palate, eyelid, face, or orbital areas.  

               c ) Primary etiology of the Rhino-orbital mucormycosis is generally diabetes from which the patient is suffering in this case.

2Q) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?
       ANS: 1) Pharmacological interventions:

Ø Inj. LIPOSOMAL AMPHOTERICIN B: It is used to treat fungal infections. It binds to ergosterol in the fungal cell membrane, which leads to formation of pores, ion leakage and ultimately fungal cell death.

Ø ITRACONAZOLE 200mg: It is also used to treat fungal infections. It acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-alpha-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis.

Ø DEOXYCHOLATE AMP B: It is used as a fungicidal. Polyenes bind to ergosterol in the fungal cell wall, disrupting the cell, altering its permeability and killing the fungus.

3Q) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 
  ANS: People with more severe forms of COVID-19 are treated with steroid medications, which can suppress the immune system, opening them up to a fungal infection like mucormycosis.

And also, people who do not maintain hygiene with masks are also being affected with mucormycosis as the unhygienic masks develop moisture which leading to this condition at this point of time.

*MEDICAL EDUCATION:

Personal experience:
This was my first online assignment and I feel happy  to be a part of this learning experience where in I could personally place myself in the place of a doctor and learn how to present a case.I have also taken part in virtual classes and understood the hisory of patients and our treatment methods.I studied thoroughly blogs of my friends. I have learnt many new things through the blogs. This helps me a lot with integrating my knowledge practically.I heartfully thank you for this opportunity and I also thank our Professor Rakesh Biswas sir and PG's for guiding us.

    







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